We continue to look at differences between nonmetastatic and metastatic variants of the MDAY-D2 tumor. To date, an analysis of at least five differences between these two phenotypes has demonstrated no correlation between any specific alteration in metabolic or surface characteristics of the tumors and their ability to metastasize. This simply reaffirms our belief that the acquisition of the metastatic phenotype requires a complex series of events. In addition, we've expanded our studies and have shown that one can select immunogenic variants from malignant tumors by mutagen treatment. The high frequency of immunogenic variant selection could be explained by recent evidence in our laboratory that 5-azacytidine also can generate immunogenic variants at high frequency, presumably by gene deregulation secondary to undermethylation of DNA. The expression of antigen by immunogenic variants is currently being analyzed using cell and microcell fusion methods.